Nutritional neuroscience · 2013
Prenatal molybdenum exposure and infant neurodevelopment in Mexican children.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Vázquez-Salas Ruth Argelia, López-Carrillo Lizbeth, Menezes-Filho José A, Rothenberg Stephen J, Cebrián Mariano E, Schnaas Lourdes, Viana Gustavo Freitas de Souza, Torres-Sánchez Luisa
Аннотация
OBJECTIVE: To evaluate the association between prenatal exposure to molybdenum (Mo) and infant neurodevelopment during the first 30 months of life.
METHODS: We selected a random sample of 147 children who participated in a prospective cohort study in four municipalities in the State of Morelos, Mexico. The children were the products of uncomplicated pregnancies with no perinatal asphyxia, with a weight of ≥2 kg at birth, and whose mothers had no history of chronic illnesses. These women were monitored before, during, and after the pregnancy. For each of these children a maternal urine sample was available for at least one trimester of pregnancy, and urine Mo levels were determined by electrothermal atomic absorption spectrometry. Neurodevelopment was evaluated using the psychomotor (PDI) and mental development indices (MDI) of the Bayley scale. Association between prenatal exposure to Mo and infant neurodevelopment was estimated using generalized mixed effect models.
RESULTS: The average urinary concentrations of Mo adjusted for creatinine varied between 45.6 and 54.0 µg/g of creatinine at first and third trimester, respectively. For each doubling increase of Mo (μg/g creatinine) during the third trimester of pregnancy, we observed a significant reduction on PDI (β = -0.57 points; P = 0.03), and no effect on MDI (β = 0.07 points; P = 0.66).
DISCUSSION: As this is the first study that suggests a potential negative association between prenatal Mo exposure and infant neurodevelopment, these results require further confirmation.
METHODS: We selected a random sample of 147 children who participated in a prospective cohort study in four municipalities in the State of Morelos, Mexico. The children were the products of uncomplicated pregnancies with no perinatal asphyxia, with a weight of ≥2 kg at birth, and whose mothers had no history of chronic illnesses. These women were monitored before, during, and after the pregnancy. For each of these children a maternal urine sample was available for at least one trimester of pregnancy, and urine Mo levels were determined by electrothermal atomic absorption spectrometry. Neurodevelopment was evaluated using the psychomotor (PDI) and mental development indices (MDI) of the Bayley scale. Association between prenatal exposure to Mo and infant neurodevelopment was estimated using generalized mixed effect models.
RESULTS: The average urinary concentrations of Mo adjusted for creatinine varied between 45.6 and 54.0 µg/g of creatinine at first and third trimester, respectively. For each doubling increase of Mo (μg/g creatinine) during the third trimester of pregnancy, we observed a significant reduction on PDI (β = -0.57 points; P = 0.03), and no effect on MDI (β = 0.07 points; P = 0.66).
DISCUSSION: As this is the first study that suggests a potential negative association between prenatal Mo exposure and infant neurodevelopment, these results require further confirmation.